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Journal of Virology, March 2004, p. 2478-2485, Vol. 78, No. 5
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.5.2478-2485.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Influence of Long Terminal Repeat and Env on the Virulence Phenotype of Equine Infectious Anemia Virus

Susan L. Payne,1* Xiao-fang Pei,1,{dagger} Bin Jia,2 Angela Fagerness,2,{ddagger} and Frederick J. Fuller2

Department of Veterinary Pathobiology, Texas A&M University, College Station, Texas 77843-4467,1 Department of Microbiology, Pathology, and Parasitology, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 276502

Received 8 May 2003/ Accepted 19 November 2003

The molecular clones pSPeiav19 and p19/wenv17 of equine infectious anemia virus (EIAV) differ in env and long terminal repeats (LTRs) and produce viruses (EIAV19 and EIAV17, respectively) of dramatically different virulence phenotypes. These constructs were used to generate a series of chimeric clones to test the individual contributions of LTR, surface (SU), and transmembrane (TM)/Rev regions to the disease potential of the highly virulent EIAV17. The LTRs of EIAV19 and EIAV17 differ by 16 nucleotides in the transcriptional enhancer region. The two viruses differ by 30 amino acids in SU, by 17 amino acids in TM, and by 8 amino acids in Rev. Results from in vivo infections with chimeric clones indicate that both LTR and env of EIAV17 are required for the development of severe acute disease. In the context of the EIAV17 LTR, SU appears to have a greater impact on virulence than does TM. EIAV17SU, containing only the TM/Rev region from the avirulent parent, induced acute disease in two animals, while a similar infectious dose of EIAV17TM (which derives SU from the avirulent parent) did not. Neither EIAV17SU nor EIAV17TM produced lethal disease when administered at infectious doses that were 6- to 30-fold higher than a lethal dose of the parental EIAV17. All chimeric clones replicated in primary equine monocyte-derived macrophages, and there was no apparent correlation between macrophage tropism and virulence phenotype.

* Corresponding author. Mailing address: Department of Pathobiology, College of Veterinary Medicine, Texas A&M University, 4467 TAMU, College Station, TX 77843-4467. Phone: (979) 458-4495. Fax: (979) 862-1147. E-mail: spayne{at}cvm.tamu.edu.

{dagger} Present address: School of Public Health, West China Medical Center, Sichuan University, Chengdu, Sichuan 610041, People's Republic of China.

{ddagger} Present address: Division of Biology, Kansas State University, Manhattan, KS 66503.

Journal of Virology, March 2004, p. 2478-2485, Vol. 78, No. 5
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.5.2478-2485.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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  • Maury, W., Thompson, R. J., Jones, Q., Bradley, S., Denke, T., Baccam, P., Smazik, M., Oaks, J. L. (2005). Evolution of the Equine Infectious Anemia Virus Long Terminal Repeat during the Alteration of Cell Tropism. J. Virol. 79: 5653-5664 [Abstract] [Full Text]  


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